Implantable device with responsive vascular and cardiac controllers

ABSTRACT

Exemplary methods are described for providing responsive vascular control with or without cardiac pacing. An implantable device with responsive vascular and cardiac controllers interprets physiological conditions and responds with an appropriate degree of vascular therapy applied as electrical pulses to a sympathetic nerve. In one implementation, an implantable device is programmed to deliver the vascular therapy in response to low blood pressure or orthostatic hypotension. The device may stimulate the greater splanchnic nerve, to effect therapeutic vasoconstriction. The vascular therapy is dynamically adjusted as the condition improves. In one implementation to benefit impaired physical mobility, vascular therapy comprises vasoconstriction and is timed to coincide with a recurring segment of the cardiac cycle. The vasoconstriction assists circulation and venous return in the lower limbs of inactive and bedridden individuals. In various implementations, cardiac pacing therapy that is synergistic with the vascular therapy may be added to augment treatment.

TECHNICAL FIELD

Subject matter presented herein generally relates to implantable medicaldevices and more particularly to an implantable device with responsivevascular and cardiac controllers.

BACKGROUND

Conventionally, implantable cardiac devices (ICDs), including“pacemakers,” have emphasized stimulating the heart. The heart issituated in a single location in the body so it is relatively easy toplace an ICD in close proximity to cardiac muscle tissue. The humanvascular system, on the other hand, includes vast networks of bloodvessels that are spread pervasively throughout the body, so it isrelatively difficult to gain ICD control of vascular muscle tissue inthe linings of arteries and veins.

Conventional ICDs have avoided or ignored controlling the vascularmuscle layers of arteries and veins for additional reasons. Cardiacmuscle tissue differs from both skeletal muscle tissue and smooth muscletissue by being quickly responsive to electrical stimulation, whereasthe smooth muscle tissue surrounding arteries and veins is relativelyslow to react. Conventional circulatory control was easily achieved bystimulating the responsive and easily accessible cardiac muscle tissue,with its largely self-contained electrical system. The smooth muscletissue of the vascular system, by comparison, was more difficult toaccess and control.

The smooth muscle layers of arteries are controlled by the sympatheticand parasympathetic nervous subsystems with control often originating inthe brain, yet not under direct conscious control. A host of hormonesand pharmaceuticals that bind to receptors on smooth muscles and exerttheir own influences can interfere with artificial electrical control ofthese smooth muscle layers.

When the body controls its own vascular system, the aforementioned layerof smooth muscle between elastic lamina (layers) of an artery typicallyopens and closes the bore or “lumen” of the artery. Closing an arteriallumen is referred to as vasoconstriction, which typically increasesblood pressure because the circulatory system has a relativelyinflexible volume capacity. Opening an arterial lumen is referred to asvasodilation and typically lowers the blood pressure.

Control over the same parameters that are ubiquitously present in manyartificial hydraulic systems can lead to more masterful treatment ofhuman circulatory diseases as well. To treat hypertension (high bloodpressure) or hypotension (low blood pressure) for example, treatmentsinclude control over the heart as pump, over the volume capacity of thesystem (for example, using diuretics), and/or over the volume of fluidin the system. By nature, a human body in good health controls thesethree factors simultaneously. For example, when increased bloodperfusion is needed for physical exertion, the body may deliver moreblood to the exercising tissues by simultaneously increasing thestrength and speed of the pumping action and raising the blood pressure,by vasoconstriction.

The sympathetic and parasympathetic subsystems, which initiatevasoconstriction and vasodilation respectively, are not limited tocontrolling mere low-level operational aspects of the body correspondingto valves and sensors in a hydraulic machine. Rather, these nervoussubsystems also play more profound roles in directing activities ofdaily living and emotions. During rest times, for example, vasodilationmaintained by the parasympathetic subsystem may direct more blood toactivities like digestion, with resultant feelings of relaxation, whileduring physical activity and stress, vasoconstriction initiated by thesympathetic subsystem may direct blood away from the digestive tract toskeletal muscles, with resultant feelings of strength and excitement.

Comprehensive control of the circulatory system, such as thataccomplished by the body itself, can provide improved treatment for manycirculatory maladies. For example, orthostatic hypotension (OSH) is acommon geriatric disorder as well as a common side effect of manymedications. It is generally described as a decrease of 10-20millimeters of mercury (mmHg) or more in systolic blood pressure whenposture changes from supine to standing—a horizontal to vertical changein posture. OSH can have neurogenic etiologies (e.g., diminishedbaroreceptor reflex); vestibular disorders; peripheral/central nervoussystem deficiencies; etc.) or non-neurogenic etiologies (e.g., cardiacpump failure, reduced blood volume, venous pooling, etc.). Devicetherapies that only elevate heart rate during an OSH episode (i.e., thattarget the non-neurogenic deficiencies) may fail if there is a lack ofvasoconstriction due to reduced baroreceptor reflex. Similarly,treatments that only stimulate vasomotor sympathetic nerves (i.e.,target only neurogenic deficiencies) may fail if there is a pronouncedpumping failure. Thus, an implantable medical device therapy that cansimultaneously compensate for both neurogenic and non-neurogenicinfluences on the circulatory system can be very advantageous intreating OSH and other disorders.

There is a need for an implantable device that takes advantage of theautonomic nervous system, resulting in simultaneous control of moretypes of muscle tissues in the circulatory system than just cardiacmuscle tissue. Such an implantable device would control the cardio andvascular components of the cardiovascular system in a more organic andcomprehensive manner than just controlling heart rate and other cardiacparameters via a conventional ICD.

SUMMARY

Implantable devices and methods are described for providing responsivevascular control with or without cardiac pacing. An implantable devicewith responsive vascular and cardiac controllers interpretsphysiological conditions and responds with an appropriate degree ofvascular therapy applied as electrical pulses to a sympathetic nerve. Inone implementation, an implantable device is programmed to deliver thevascular therapy in response to low blood pressure or orthostatichypotension. The device may stimulate the greater splanchnic nerve, toeffect therapeutic vasoconstriction. The vascular therapy is dynamicallyadjusted as the condition improves.

In one implementation that is capable of benefiting a person afflictedwith impaired physical mobility, the vascular therapy to be appliedcomprises vasoconstriction, especially in the arteries of the lowerlimbs, and is timed to coincide with a recurring segment of each cardiaccycle, that is, many times per minute. The vasoconstriction is timed tooccur just as blood pressure is dropping between systole and diastole—togive the contraction of elastic arterial walls extra force. Thisprovides reinforcement for blood transport in the lower limbs of aninactive person, augmenting venous return.

In various implementations, cardiac pacing therapy that is synergisticwith the vascular therapy may be added to augment treatment. The addedcardiac pacing therapy may base values for cardiac pacing parameters onthe magnitude of current vascular stimulation parameters. If cardiactherapy is added, then both the vascular therapy and the cardiac therapycan be dynamically adjusted through feedback from physiological sensorsas conditions improve.

BRIEF DESCRIPTION OF THE DRAWINGS

FIG. 1 is a diagram illustrating an exemplary implantable device inelectrical communication with a human heart.

FIG. 2 is a diagram illustrating the exemplary implantable device inelectrical communication with a human greater splanchnic nerve.

FIG. 3 is a diagram illustrating the relative bodily position of a cuffelectrode of the exemplary implantable device around the greatersplanchnic nerve.

FIG. 4 is block diagram of an exemplary implementation of the exemplaryimplantable device.

FIG. 5 is a block diagram of an exemplary cardiovascular controller ofthe exemplary implantable device.

FIG. 6 is a diagram illustrating an exemplary therapeutic response bythe exemplary implantable device to orthostatic hypotension.

FIG. 7 is a flow diagram of an exemplary process for providingresponsive vascular therapy.

FIG. 8 is a flow diagram of an exemplary method of providing responsivecardiovascular therapy for orthostatic hypotension.

DETAILED DESCRIPTION

Overview

The following discussion describes an exemplary implantable device(“device”) that includes a responsive cardiovascular controller. Thedevice can exert artificial vasomotor control and artificial cardiaccontrol, with both cardio control and vascular control responsive toeach other and to feedback from physiological sensors. In oneimplementation, the device is capable of monitoring changes in posturesand blood pressure, and responding to these physiological variables byexerting vasomotor control, monitoring cardiac activity, and providingcardiac pacing when needed. The device includes feedback controlmechanisms that can determine the level and duration of vasomotorstimulation to apply with or without cardiac pacing to achieveappropriate vasoconstriction, cardiac pumping, and blood pressure.

In one implementation, the implantable device can control vascular tone(and cardiac pacing) in dynamic response to orthostatic hypotension. Inanother or the same implementation, the implantable device can controlvascular tone to assist blood flow in the extremities of a bedriddenperson, in response to the physiological parameter of impaired physicalmobility. In these implementations a cardiac stimulator can be includedto augment and reinforce control of vascular tone by additionallycontrolling heart rate and/or other cardiac parameters.

The aforementioned orthostatic hypotension results when a susceptibleperson assumes an upright position so that the head and brain, being atthe highest aspect of a hydrostatic column of fluid, suffer low bloodpressure causing lightheadedness and even loss of consciousness. Thesympathetic nervous system normally senses the change in blood pressureand compensates by reflexively constricting blood vessels to increasesystem pressure. Conventional techniques that compensate for orthostatichypotension have been proposed, for example, in U.S. Pat. No. 4,791,931to Slate, entitled, “Demand pacemaker using an artificial baroreceptorreflex.” The Slate technique, however, increases only heart rate tocompensate for low blood pressure. A natural baroreceptor reflex alsoincreases vascular tone in response to intracranial blood pressure thathas decreased too quickly. This vasoconstriction decreases the volume ofthe arterial circulatory system thereby increasing fluid pressure to thehead.

Some individuals lack a normal baroreceptor reflex so that aconventional technique, such as that described by Slate—of increasingheart rate to compensate for orthostatic hypotension—is not effective.Implementations of the implantable device described herein can sensechanges in blood pressure through conventional methods and, beingalerted to an undesirable condition, can initiate a compensatory changein vascular tone that is proportional to the initial degree of bloodpressure change and dynamically maintain treatment for ongoingvariations thereafter. Moreover, blood pressure sensing—or more broadly,sensing of a physiologic variable—and the responsive vascular tonecontrol are coupled in a feedback loop that models the human body's ownfeedback mechanisms for regulating body systems and maintainingphysiological homeostasis. Since the implantable device can controlvascular tone, various alternative implementations of the device may beused to assist blood flow in bedridden individuals or provide therapyfor other vascular conditions, such as peripheral vascular disease ofdiabetes, vasovagal syncope, post-fracture swelling of a limb due tolack of muscular and vascular tone after casting, etc.

Exemplary Implantable Device

FIG. 1 shows an exemplary implementation of the device 100 introducedabove in electrical communication with a human heart 102 and otherbodily tissues. Such an exemplary device 100 can be characterized as aminiature computing device that is implanted into a body to monitor,regulate, and/or correct cardiovascular and other activities. The device100 may be an ICD (e.g., implantable cardiac pacemaker, implantabledefibrillator, etc.) that applies stimulation therapy to the heart ormay be another type of implantable device that can perform theresponsive cardiovascular techniques described herein. In theillustrated implementation, three of the electrical leads—a right atriallead 104, a coronary sinus lead 106, and a right ventricular lead108—interconnect the device 100 with the heart 102 to supportmulti-chamber detection and stimulation therapy. One or morephysiological sensor lead(s) 110 may also be employed to positionphysiological sensors within the body and a vascular stimulation lead112 may be used to position electrodes to facilitate stimulation ofvascular tissue or nervous tissue that innervates a vascular bed.

The right atrial lead 104 supports an atrial tip electrode 120, which istypically implanted in a patient's right atrial appendage. The rightatrial lead 104 also supports a right atrial ring electrode 121, whichenables the device to sense atrial cardiac signals and apply pacingtherapy to the right atrial chamber.

The coronary sinus lead 106 positions a left ventricular tip electrode122 adjacent to the left ventricle and/or additional electrode(s)adjacent to the left atrium, such as a left atrial ring electrode 124and a left atrial coil electrode 126. The coronary sinus lead 106enables the exemplary device 100 to sense left atrial and ventricularcardiac signals and administer left chamber pacing therapy. In theillustrated arrangement, the left ventricular tip electrode 122 is usedto sense atrial and ventricular cardiac signals and deliver leftventricular pacing therapy. The left atrial ring electrode 124 isemployed for applying left atrial pacing therapy, and the left atrialcoil electrode 126 may be used for shocking therapy.

The right ventricular lead 108 is electrically coupled to a rightventricular tip electrode 128, a right ventricular ring electrode 130, aright ventricular (RV) coil electrode 132, and a superior vena cava(SVC) coil electrode 134. Typically, the right ventricular lead 108 istransvenously inserted into the heart 102 to place the right ventriculartip electrode 128 in the right ventricular apex so that the RV coilelectrode 132 will be positioned in the right ventricle and the SVC coilelectrode 134 will be positioned in the superior vena cava. Accordingly,the right ventricular lead 108 is capable of receiving cardiac signals,and delivering stimulation in the form of pacing and shock therapy tothe right ventricle.

One or more physiological sensor lead(s) 110 may be positioned to allowa physiological sensor 140, such as a blood pressure probe, to come incontact with the patient's blood, nerve tissue, or other bodily part. Inthe case of a blood pressure probe, a photoplethysmograph (PPG) infraredlight sensor may be coupled to the physiological sensor lead 110.

A vascular stimulation lead 112 may be positioned to facilitatestimulation of vascular tissue or nervous tissue that innervates avascular bed. The nervous tissue may be a sympathetic efferent nerve,such as the greater splanchnic nerve. If one or more sympathetic nervesare to be stimulated to control vascular tone, then one or more cuffelectrodes 142 may be used to couple the vascular stimulation lead 112to the nerve tissue.

FIG. 2 shows an exemplary placement of a cuff electrode 142 on asympathetic nerve, such as the greater splanchnic nerve 200, tostimulate the nerve and achieve a vasomotor response.

The greater splanchnic nerve 200 is the preganglionic sympatheticinnervation to the celiac ganglia 202, which typically lie on orstraddle the inferior aorta. The celiac ganglia 202 lie on the left andright sides of the celiac trunk at its origin and are in contact withthe surface of the aorta. They are the largest of the sympatheticganglia that are located on the aorta's surface. The celiac ganglia 202innervate various abdominal organs and glands (e.g., the liver, stomach,pancreas, kidneys, and small intestine). It should be noted that nerveimpulses through sympathetic fibers to these visceral organs generallyinhibit the activity of the organs. The celiac ganglia 202 also provideinnervation to the adrenal glands and to the abdominal splanchnicvascular bed 204. This vascular bed may be the major effector mechanismfor the arterial baroreflex. That is, in a healthy individual, low bloodpressure triggers a baroreceptor reflex that sends sympathetic nerveimpulses to the adrenal glands and to the abdominal splanchnic vascularbed 204 in order to compensate for the low blood pressure. Thecompensation likely comprises a global vasoconstriction of the vesselsin the abdominal splanchnic vascular bed 204 and a release ofepinephrine from the adrenal glands.

The release of epinephrine (adrenaline) into the circulatory system inresponse to splanchnic nerve stimulation produces a pronounced globalsympathetic effect that causes vasoconstriction and increases bloodpressure in most parts of the body almost instantaneously. Thus, bystimulating the greater splanchnic nerve 200, the device 100 effects avasomotor response electrically, mechanically (throughvasoconstriction), and chemically (through release of epinephrine).

FIG. 3 shows an exemplary placement of the vascular stimulation lead 112in relation to other aspects of the human body. A cuff electrode 142 isshown surgically placed around the greater splanchnic nerve 200. Thevascular stimulation lead 112, or course, couples one or more cuffelectrodes 142 with the device 100 (not shown, because the device 100may be placed in various locations, for example, it may even be placedin the abdomen).

FIG. 4 shows an exemplary block diagram depicting various components ofthe device 100. The components are typically contained in a case 400,which is often referred to as the “can”, “housing”, “encasing”, or “caseelectrode”, and may be programmably selected to act as the returnelectrode for unipolar operational modes. The case 400 may further beused as a return electrode alone or in combination with one or more ofthe coil electrodes 126, 132 and 134 for stimulating purposes. The case400 further includes a connector (not shown) having a plurality ofterminals (401, 402, 404, 406, 408, 412, 414, 415, 416, 417, and419—shown schematically with the names of the electrodes to which theyare connected shown next to the terminals), including:

-   -   a right atrial ring terminal (AR RING) 401 for atrial ring        electrode 121;    -   a right atrial tip terminal (AR TIP) 402 for atrial tip        electrode 120;    -   a left ventricular tip terminal (VL TIP) 404 for left        ventricular tip electrode 122;    -   a left atrial ring terminal (AL RING) 406 for left atrial ring        electrode 124;    -   a left atrial shocking terminal (AL COIL) 408 for left atrial        coil electrode 126;    -   a right ventricular tip terminal (VR TIP) 412 for right        ventricular tip electrode 128;    -   a right ventricular ring terminal (VR RING) 414 for right        ventricular ring electrode 130;    -   a right ventricular shocking terminal (RV COIL) 415 for RV coil        electrode 132;    -   an SVC shocking terminal (SVC COIL) 416 for SVC coil electrode        134;    -   a physiological sensor terminal 417 for physiological sensor        140, e.g., a blood pressure probe; and    -   a vascular stimulation terminal 419 for coupling with a vascular        stimulation lead 112 and cuff electrode.

An exemplary device 100 may include a programmable microcontroller 420that controls various operations of the implantable cardiac device,including cardiac monitoring and cardiovascular stimulation therapy.Microcontroller 420 includes a microprocessor (or equivalent controlcircuitry), RAM and/or ROM memory, logic and timing circuitry, statemachine circuitry, and I/O circuitry.

Exemplary device 100 further includes an atrial pulse generator 422 anda ventricular pulse generator 424 that generate pacing stimulationpulses for delivery by the right atrial lead 104, the coronary sinuslead 106, and/or the right ventricular lead 108 via an electrodeconfiguration switch 426. The electrode configuration switch 426 mayinclude multiple switches for connecting the desired electrodes to theappropriate I/O circuits, thereby providing complete electrodeprogrammability. Accordingly, switch 426, in response to a controlsignal 427 from the microcontroller 420, determines the polarity of thestimulation pulses (e.g., unipolar, bipolar, etc.) by selectivelyclosing the appropriate combination of switches.

To provide stimulation therapy in each of the four chambers of theheart, the atrial and ventricular pulse generators 422 and 424 mayinclude dedicated, independent pulse generators, multiplexed pulsegenerators, or shared pulse generators. The pulse generators 422 and 424are controlled by the microcontroller 420 via appropriate controlsignals 428 and 430, respectively, to trigger or inhibit the stimulationpulses.

Microcontroller 420 is illustrated as including timing control circuitry432 to control the timing of the stimulation pulses (e.g., pacing rate,atrioventricular (AV) delay, atrial interconduction (A-A) delay, orventricular interconduction (V-V) delay, native atrial event to nativeor stimulated ventricular event (PV) delay, (AV/PV) delay, etc.). Thetiming control circuitry may also be used for the timing of refractoryperiods, blanking intervals, noise detection windows, evoked responsewindows, alert intervals, marker channel timing, and so on.

Microcontroller 420 may also implement an arrhythmia detector 434, amorphology detector 436, and an exemplary cardiovascular controller 438.The cardiovascular controller 438 in turn can process input fromphysiological sensors 470, such as accelerometers and a blood pressuresensor 473, diagnose cardiovascular disturbances, such as orthostatichypotension, and provide cardiovascular therapies. The therapies maycompensate for detected cardiovascular disturbances using ongoingfeedback from the physiological sensors 470. The cardiovascularcontroller 438 can also provide synergistic vascular and cardiactherapies.

The components 434, 436, and 438 may be implemented in hardware as partof the microcontroller 420, or as software/firmware instructionsprogrammed into an implementation of the device 100 and executed on themicrocontroller 420 during certain modes of operation. Although notshown, the microcontroller 420 may further include other dedicatedcircuitry and/or firmware/software components that assist in monitoringvarious conditions of the patient's heart and managing pacing therapies.

Atrial sensing circuits 444 and ventricular sensing circuits 446 mayalso be selectively coupled to the right atrial lead 104, coronary sinuslead 106, and the right ventricular lead 108, through the switch 426 todetect the presence of cardiac activity in each of the four chambers ofthe heart. The sensing circuits 444 and 446 may include dedicated senseamplifiers, multiplexed amplifiers, or shared amplifiers. Switch 426determines the “sensing polarity” of the cardiac signal by selectivelyclosing the appropriate switches. In this way, the clinician may programthe sensing polarity independent of the stimulation polarity.

Each sensing circuit 444 and 446 may employ one or more low powerprecision amplifiers with programmable gain and/or automatic gaincontrol, bandpass filtering, and a threshold detection circuit toselectively sense the cardiac signal of interest. The automatic gaincontrol enables the exemplary device 100 to sense low amplitude signalcharacteristics of atrial or ventricular fibrillation.

The outputs of the atrial and ventricular sensing circuits 444 and 446are connected to the microcontroller 420 which, in turn, is able totrigger or inhibit the atrial and ventricular pulse generators 422 and424 in a demand fashion in response to the absence or presence ofcardiac activity in the appropriate chambers of the heart. The sensingcircuits 444 and 446 receive control signals from the microcontroller420 over signal lines 448 and 450 to control, for example, the gainand/or threshold of polarization charge removal circuitry (not shown)and the timing of blocking circuitry (not shown) optionally coupled tothe inputs of the sensing circuits 444, 446.

Cardiac signals are supplied to an analog-to-digital (ND) dataacquisition system 452, which is configured to acquire intracardiacelectrogram signals, convert the raw analog data into a digital signal,and store the digital signals for later processing and/or telemetrictransmission to an external device 454. The data acquisition system 452is coupled to the right atrial lead 104, the coronary sinus lead 106,and the right ventricular lead 108 through the switch 426 to samplecardiac signals across any pair of desired electrodes.

The data acquisition system 452 is coupled to the microcontroller 420,or other detection circuitry, to assist in detecting an evoked responsefrom the heart 102 in response to an applied stimulus, which is oftenreferred to as detecting “capture”. Capture occurs when an electricalstimulus applied to the heart is of sufficient energy to depolarize thecardiac tissue, thereby causing the heart muscle to contract. Themicrocontroller 420 detects a depolarization signal during a windowfollowing a stimulation pulse, the presence of which indicates thatcapture has occurred. The microcontroller 420 enables capture detectionby triggering the ventricular pulse generator 424 to generate astimulation pulse, starting a capture detection window using the timingcontrol circuitry 432 within the microcontroller 420, and enabling thedata acquisition system 452 via control signal 456 to sample the cardiacsignal that falls in the capture detection window and, based on theamplitude, determines if capture has occurred.

The microcontroller 420 is further coupled to a memory 460 by a suitabledata/address bus 462. The programmable operating parameters used by themicrocontroller 420 are stored in memory 460 and used to customize theoperation of the exemplary device 100 to suit the needs of a particularpatient. Such operating parameters define, for example, pacing pulseamplitude, pulse duration, electrode polarity, rate, sensitivity,automatic features, arrhythmia detection criteria, and the amplitude,waveshape and vector of each shocking pulse to be delivered to thepatient's heart 102 within each respective tier of therapy.

The operating parameters of the exemplary device 100 may benon-invasively programmed into the memory 460 through a telemetrycircuit 464 in telemetric communication via communication link 466 withthe external device 454, such as a programmer, local transceiver, or adiagnostic system analyzer. The microcontroller 420 can activate thetelemetry circuit 464 with a control signal 468. The telemetry circuit464 allows intracardiac electrograms and status information relating tothe operation of the exemplary device 100 (as contained in themicrocontroller 420 or memory 460) to be sent to the external device 454through an established communication link 466.

The physiological sensors 470 referred to above can further include, forexample, “rate-responsive” sensors that adjust pacing stimulation ratesaccording to the exercise state of the patient. Accordingly, themicrocontroller 420 responds by adjusting the various pacing parameters(such as rate, AV Delay, V-V Delay, etc.) at which the atrial andventricular pulse generators 422 and 424 generate stimulation pulses.

The physiological sensors 470 may include mechanisms and sensors todetect bodily movement, changes in cardiac output, changes in thephysiological condition of the heart, diurnal changes in activity (e.g.,detecting sleep and wake states), G-force acceleration of the pacemakercase 400, length of the cardiac QT interval, blood oxygen saturation,blood pH, changes in blood pressure, changes in temperature, respirationrate, and QRS wave duration. While shown as being included within theexemplary device 100, the physiological sensor(s) 470 may also beexternal to the exemplary device 100, yet still be implanted within orcarried by the patient, e.g., a blood pressure probe. Examples ofphysiological sensors external to the case 400 that may be deployed bydevice 100 include sensors that, for example, sense respirationactivities, O2 saturation, evoked response, pH of blood, and so forth.

The illustrated physiological sensors 470 include one or moreactivity/position sensors 471 (e.g., 1D or 3D accelerometers, movementsensors, etc.) to detect changes in the patient's position. Theactivity/position sensors 471 can be used by a cardiovascular controller438 to assist detection of orthostatic hypotension caused by transitionfrom a less upright posture to a comparatively more upright posture. Oneexample postural change leading to orthostatic hypotension insusceptible individuals is a movement from a supine position in a reststate (e.g., sleeping in bed) to an upright position in a non-rest state(e.g., sitting or standing up). In response to the detected posturalchange, a cardiovascular controller 438 may evaluate blood pressure tosee if there has been a decrease in the blood pressure sustained for aduration that is longer than that which usually transpires before ahealthy baroreceptor reflex intervenes. The cardiovascular controller438 may then administer one or more vascular and/or pacing therapies toreduce the orthostatic hypotension.

In one configuration, accelerometer output signal is bandpass-filtered,rectified, and integrated at regular timed intervals. A processedaccelerometer signal can be used as a raw activity signal. The devicederives an activity measurement based on the raw activity signal atintervals timed according to the cardiac cycle. The activity signalalone can be used to indicate whether a patient is active or resting.The activity measurement can further be used to determine an activityvariance parameter. A large activity variance signal is indicative of aprolonged exercise state. Low activity and activity variance signals areindicative of a prolonged resting or inactivity state. The activityvariance can be monitored diurnally to detect the low variance in themeasurement corresponding to the sleep state. For a complete descriptionof the activity variance sensor, the reader is directed to U.S. Pat. No.5,476,483 (Bornzin et al.), issued Dec. 19, 1995, which is herebyincorporated by reference.

Other illustrated physiological sensors 470 include one or more bloodpressure sensors 473, such as a photoplethysmograph (PPG) infrared lightsensor surface mounted on the case 400 or external to the device 100.Thus, signals generated by the physiological sensors 470 can be passedto the microcontroller 420 for analysis by the cardiovascular controller438. Such signals can be used to determine whether the patient is atrest, whether the patient is experiencing an episode of orthostatichypotension or other cardiovascular disturbance and whether to invokeany responsive therapy prescribed by the cardiovascular controller 438.

A minute ventilation (MV) sensor 472 may also be included in thephysiological sensors 470 in order to sense rate and depth of breathing.Minute ventilation can be measured as the total volume of air that movesin and out of a patient's lungs in a minute. The MV sensor 472 may usetransthoracic impedance, which is a measure of impedance across thechest cavity, to sense air movement.

The exemplary device 100 additionally includes a battery 476 thatprovides operating power to all of the components shown in FIG. 4. Thebattery 476 is capable of operating at low current drains for longperiods of time (e.g., less than 10 μA), and is capable of providinghigh-current pulses (for capacitor charging) when the patient requires ashock pulse (e.g., in excess of 2 A, at voltages above 2 V, for periodsof 10 seconds or more). The battery 476 also desirably has predictabledischarge characteristics so that elective replacement time can bedetected. As one example, the exemplary device 100 employslithium/silver vanadium oxide batteries.

The exemplary device 100 can further include magnet detection circuitry(not shown), coupled to the microcontroller 420, to detect when a magnetis placed over the exemplary device 100. A magnet may be used by aclinician to perform various test functions of the exemplary device 100and/or to signal the microcontroller 420 that an external programmer(e.g., 454) is in place to receive or transmit data to themicrocontroller 420 through the telemetry circuits 464.

The exemplary device 100 further includes an impedance measuring circuit478 that is enabled by the microcontroller 420 via a control signal 480.The impedance measuring circuit 478 is used for many things, including:lead impedance surveillance during acute and chronic phases for properlead positioning or dislodgement; detecting operable electrodes andautomatically switching to an operable pair if dislodgement occurs;measuring respiration or minute ventilation; measuring thoracicimpedance for determining shock thresholds; detecting when the devicehas been implanted; measuring cardiac stroke volume; detecting theopening of heart valves; and so forth. The impedance measuring circuit478 may be coupled to the switch 426 so that any desired electrode maybe used.

The exemplary device 100 may be operated as an implantablecardioverter/defibrillator device, which detects the occurrence of anarrhythmia and automatically applies an appropriate electrical shocktherapy to the heart aimed at terminating the detected arrhythmia. Tothis end, the microcontroller 420 further controls a shocking circuit482 via a control signal 484. The shocking circuit 482 generatesshocking pulses of low (e.g., up to 0.5 joules), moderate (e.g., 0.5-10joules), or high energy (e.g., 11 to 40 joules), as selected by themicrocontroller 420. Such shocking pulses are applied to the patient'sheart 102 through at least two shocking electrodes selected, forexample, from the left atrial coil electrode 126, the RV coil electrode132, and/or the SVC coil electrode 134. As noted above, the case 400 mayact as an active electrode in combination with the RV electrode 132, oras part of a split electrical vector using the SVC coil electrode 134 orthe left atrial coil electrode 126 (i.e., using the RV electrode as acommon electrode).

Cardioversion shocks are generally considered to be of low to moderateenergy level (so as to minimize pain felt by the patient), and/orsynchronized with an R-wave and pertain to the treatment of tachycardia.Defibrillation shocks are generally of moderate to high energy level(i.e., corresponding to thresholds in the range of, e.g., 5-40 joules),delivered asynchronously (since R-waves may be too disorganized), andpertain exclusively to the treatment of fibrillation. Accordingly, themicrocontroller 420 is capable of controlling the synchronous orasynchronous delivery of the shocking pulses.

More generally, the exemplary device 100 can be programmed to stimulatedifferent sets of vascular and cardiac muscles through the samelead/electrode system. The exemplary device 100 can be programmed tovary the output voltage of various pulses to effectively stimulatedifferent muscles of the heart and blood vessels, even though the leadand electrode placement does not change.

Exemplary Cardiovascular Controller

FIG. 5 shows an exemplary cardiovascular controller 438 that can beimplemented in an implantable medical device, such as device 100. Thecomponents of a cardiovascular controller 438, communicatively coupledwith each other and with control logic 500, can be implemented insoftware, hardware, firmware, etc., or combinations thereof.

As mentioned, cardiovascular controller 438 has access to or includesphysiological sensors 470. The physiological sensors 470 selected for agiven implementation depend on the condition being treated. If thecondition is orthostatic hypotension, then an activity/position sensor471 that likely includes accelerometers may be included. A bloodpressure sensor 473 and/or blood pressure probe may be included. Aphysiologic interpreter 502 can receive input from the physiologicalsensors 470 and interpret the input to diagnose a condition to betreated. The physiologic interpreter 502 provides feedback regardingchanges in the condition being treated to the cardiovascular controller438 and thereby provides information regarding the efficacy of therapiesbeing provided by the cardiovascular controller 438. A timer 504 isincluded in the physiologic interpreter 502 to measure changes in thecondition being treated and/or the efficacy of therapy over a timeinterval.

An exemplary vascular therapy controller 506 included in thecardiovascular controller 438 receives physiological information fromthe physiologic interpreter 502 and alters vascular stimulationresponsively. Since the timer 504 can allow detection of physiologicalchanges over very short time intervals, the vascular therapy controller506 can dynamically match a given vascular therapy to changingconditions in near real time. For example, if a blood pressure sensorupdates its readout approximately every 100 milliseconds, then thevascular therapy controller 506 can follow the blood pressure changeswith an algorithm that changes vascular stimulation in proportion tochanges in blood pressure, many times per second.

In one implementation, the vascular therapy controller 506 includes avascular tone selector 508, a correlation table 510, and a stimulationselector 512. Vascular tone refers to a degree of vasoconstriction orvasodilation. The vascular tone selector 508 aims to select or calculatea degree of vascular tone that compensates or is therapeutic for a givencondition. If the condition being treated is hypotension, then thevascular tone selector 508 seeks to increase blood pressure by promotingvasoconstriction. If the condition being treated is hypertension,however, then the vascular tone selector 508 may seek to decrease bloodpressure by attenuating or foregoing vascular stimulation.

The correlation table 510 associates a physiological change in statedetermined by the physiologic interpreter 502 with a therapeuticresponse. For example, a sudden drop in blood pressure may be correlatedwith a particular voltage for stimulating a compensatory vascularresponse. Likewise, a particular vasomotor response selected by thevascular tone selector 508 may be correlated with stimulation parameterscapable of achieving the vasomotor response. If the correlation table510 does not yield vascular stimulation parameters directly, then astimulation selector 512 may be included to convert a correlationintermediate to definite electrical quantities for performing thevascular stimulation. In other words, there may be a chain of relatedintermediate parameters between a physiological change detected by thephysiologic interpreter 502 and the actual electrical quantities to beapplied as responsive therapy for the physiological change.

In one implementation, the vascular correlation table 510 is included inor replaced by a correlation engine that executes an algorithm relatinga detected physiological change to parameters for executing a vascularstimulation therapy. In another implementation, the vascular therapycontroller 506 solves an equation at regular intervals in which aphysiological variable on one side of the equation is proportional to astimulation parameter on the other side of the equation. In yet anotherimplementation, the vascular tone selector 508 and/or the vascularstimulation selector 512 may be excluded if their functions can beincorporated into a vascular correlation table 510 that is completeenough, e.g., that contains precalculated relationships between multipleintermediate variables.

Once the vascular therapy controller 506 selects stimulation parameters,a vascular stimulator 514 applies the stimulation to target tissue. Ifthe target tissue is the greater splanchnic nerve 200, then electricalpulses may be applied through a vascular stimulation lead 112 and a cuffelectrode 142. In the exemplary device 100, the shocking circuits 482may include the vascular stimulator 514 as well as a cardiac stimulator516.

Some implementations of the cardiovascular controller 438 may alsoinclude a cardiac therapy controller 518. In one implementation, thecardiac therapy controller 518 responds independently to feedback fromthe physiologic interpreter 502. In another implementation the cardiactherapy controller 518 determines a therapy based on the stimulationparameters determined by the vascular therapy controller 506. In yetanother implementation, the cardiac therapy controller 518 considersinput from both the physiologic interpreter 502 and the vascular therapycontroller 506 in determining a cardiac therapy. The cardiac therapycontroller 518 augments the vascular stimulation of the vascular therapycontroller 506 in achieving a cardiovascular treatment or in some casesthe two controllers (506, 518) work in concerted interdependence on eachother.

A cardiac therapy controller 518 typically monitors cardiac activitythrough conventional components of a host ICD or even via components ofa physiologic interpreter 502. Even so, the cardiac therapy controller518 is not identical to a conventional ICD (e.g., for pacemaking)although functionality of the two may greatly overlap in some cases,especially when a cardiac therapy controller 518 utilizes the resourcesof an ICD to perform its functions. The cardiac therapy controller 518can sometimes be differentiated from conventional ICDs in that thecardiac therapy controller 518 is more narrowly focused on the samecardiovascular treatment goal as the vascular therapy controller 506 andthe stimulation parameter values selected by the cardiac therapycontroller 508 are often derived from or interdependent on thestimulation parameter values selected by the vascular therapy controller506. In other words, the two controllers (506, 518) team up to treat aspecific cardiovascular condition using interdependent cardio andvascular stimulation parameters.

The cardiac therapy controller 518 may include a cardiac parameter valueselector 520 (e.g., a heart rate selector) that proposes a value for acardiac parameter to augment the compensatory vascular stimulationarrived at by the vascular therapy controller 506. The cardiac parametervalue may also be selected in response to feedback provided by thephysiologic interpreter 502, as discussed above.

The cardiac therapy controller 518 may include a cardiac correlationtable 522 and a cardiac stimulation selector 524. These two componentsfunction analogously to the vascular correlation table 510 and thevascular stimulation selector 512 discussed above, namely, theytranslate a cardiac therapy enjoined in order to augment a vasculartherapy into specific values of electrical parameters for applyingcardiac stimulation. Like the vascular therapy controller 506 discussedabove, in one implementation the cardiac parameter value selector 520and/or the cardiac stimulation selector 524 may be excluded. This occursif their functions can be incorporated into a cardiac correlation table522 that is comprehensive enough to include precalculated relationshipsbetween related intermediate parameters that link the physiologicalcondition being treated to values for electrical parameters for applyingthe augmentative cardiac stimulation.

The cardiac correlation table 522 and other components may be replacedby an engine that runs an exemplary cardiac correlation algorithm,relating a proposed cardiac response to the electrical quantities thatcan effect the response. In general, the cardiac therapy controller 518is responsive to ongoing changes in the cardiovascular condition beingtreated and is also dynamically responsive to the ongoing adjustmentsbeing made by the vascular therapy controller 506.

FIG. 6 shows an exemplary therapy responsive to orthostatic hypotension.The therapy is provided by components of an exemplary device 100depicted in FIGS. 1-5. Specifically, a cardiovascular controller 438 asdepicted in FIG. 5 provides a response to an initial detection oforthostatic hypotension and thereafter dynamically tailors the ongoingtherapy to subsequent changes in the orthostatic hypotension.

When a susceptible person 600 assumes a bodily position of increasedverticality with respect to gravity, the emerging (higher) hydrostaticcolumn of bodily fluids is influenced by the pull of gravity faster thanbodily reflexes can compensate, resulting in a sudden drop inintracranial blood pressure. The change in bodily position may bedetected by an accelerometer or activity/position sensor 471 in thedevice 100 and the decrease in blood pressure may be detected by aphysiological sensor 140, by a blood pressure sensor 473, and/orphysiologic interpreter 502. A timer 504 may commence a measurementinterval (for example, half a second) at the end of which the bloodpressure is reevaluated. If the blood pressure is still unsatisfactory,then the device 100 may intervene at the end of the time interval, i.e.,before the susceptible person 600 faints. The combination of detecting aqualifying body position and a sudden decrease in blood pressuresustained over the time interval provides a trigger for activating thevascular therapy controller 506.

In an example of a vascular correlation table 510, the illustratedimplementation depicts a family of precalculated relationships betweenpossible changes in the physiological condition being treated andcorresponding values for electrical parameters. The values for each setof electrical parameters represent controlled responses to be used forapplying electro-stimulation to a sympathetic nerve, e.g., to thegreater splanchnic nerve 200, in order to elicit rapid globalvasoconstriction that mimics a healthy baroreceptor reflex. Uponassuming a more upright position, if the systolic blood pressure of thesusceptible person 600 drops from, e.g., 120 mmHg to 110 mmHg (an 8%decrease), and the lower blood pressure reading is sustained for arequisite time interval, then the vascular therapy controller 506 istriggered and the vascular correlation table 510 is referenced at theentry or record for the 8% decrease in blood pressure.

In the shown implementation, percentage changes in blood pressure arecorrelated directly with values for electrical parameters forstimulating the greater splanchnic nerve 200. For example, in a givensusceptible person 600, an orthostatic hypotension episode with aninitial blood pressure drop of 8% may call for a therapy consisting of atrain of sympathetic electro-pulses in which the train includes threevolt pulses of one millisecond duration each that have an energy of onehundred nanojoules apiece, applied to the greater splanchnic nerve 200at a frequency of twenty pulses per second (Hz); the train of pulseslasting 250 milliseconds. This would apply a train of approximately fourpulses before the occurrence of a subsequent reevaluation of bloodpressure using feedback from the physiologic interpreter 502.

If the initial drop in blood pressure is greater than 8%, then thevascular therapy controller may begin treatment with a greater vascularresponse magnitude (i.e., higher voltage, higher frequency, and/orlonger pulse train). Then, as the applied therapy has its beneficialeffect the vascular therapy controller 506 adjusts treatment byreferencing the vascular correlation table 510 at the entry or record ofthe current value of blood pressure change—provided as feedback by thephysiologic interpreter 502. It should be noted that the percentagechange calculation may use an initial blood pressure value 604 for thecalculations.

The magnitude of a vascular therapy response can be fed as input to thecardiac therapy controller 518. It should be noted that someimplementations of the cardiovascular controller 438 do not include acardiac therapy controller 518 at all. The cardiac correlation table 522relates the input vascular response magnitude 606 to a value for acardiac parameter in order to create a cardiac stimulation that augmentsor is synergistic with the vascular stimulation to be applied (oralready being applied).

For example, a slight drop in blood pressure might elicit values forelectrical parameters from the vascular therapy controller 506 thatcorrelate with a cardiac pacing rate of 70 beats per minute—to be usedif the native pulse rate is below this nominal value. The value forproposed pacing rate might increase in conjunction with proposedincreases in the vascular response magnitude 606.

The vascular and cardiac stimulation values are passed respectively tothe vascular stimulator 514 and to the cardiac stimulator 516, andthence to the respective tissues. The stimulation therapies applied havea physiological effect or lack thereof that is detected by thephysiologic interpreter 502 (in this case, a blood pressure changeinterpreter). The detected physiological changes are provided asfeedback to the vascular therapy controller 506, as already discussed,to forge a subsequent vascular response, that is, an adjustment of thetherapy. Thus, the various phases of the example therapeutic response toorthostatic hypotension comprise a self-regulating feedback circuit 608that dynamically adjusts itself to cover whatever changes happen in thephysiological condition being treated.

In an alternative implementation, a cardiovascular controller 438 isprogrammed to provide vascular stimulation via a sympathetic nerve forimproving circulation in bedridden and inactive persons. Avasoconstriction response is nearly instantaneous when the vascularstimulator 514 applies pulses to the greater splanchnic nerve 200 (e.g.,the above-mentioned indirect releases of epinephrine are known to have aglobal effect on blood vessels that is nearly instantaneous—that is,each release is a tiny “adrenaline rush”). Bursts of vascularstimulation pulses can be timed to coincide with one or more points orsegments in the cardiac cycle in order to reinforce blood circulation,especially in the lower limbs of a person who is bed-bound. It is wellknown that the contraction of leg muscles used during ambulation assiststhe pumping action of the heart, especially by pushing blood throughvenous valves. This alternative implementation augments the pumpingaction of the heart in an inactive person. A similar implementation maytreat persons afflicted with diastolic heart failure.

In the above-described alternative implementation, the physiologicinterpreter 502 may monitor the cardiac cycle and the implementationtimes a vascular stimulation burst to coincide with a segment of thecardiac cycle at which systole is waning into diastole. At this or someother cardiac segment determined by trial-and-error (as their may besome lag in the responsiveness of the vascular system), the vasculartherapy controller 506 applies pulses so that vasoconstriction occursjust as blood pressure is dropping between systole and diastole—to givethe contraction of elastic arterial walls an extra boost. This providesan extra motor for circulation in the lower limbs of an inactive personby augmenting venous return.

Exemplary Methods

FIG. 7 shows an exemplary process 700 for dynamically providing avascular response to one or more physiological conditions. This process700 may be implemented in connection with any suitably configureddevice, although it will be described as being executed by the exemplaryimplantable device 100 of FIGS. 1-6. In the flow diagram of FIG. 7, theoperations are summarized in individual blocks. The operations may beperformed in hardware and/or as machine-readable instructions (softwareor firmware) that can be executed by a processor, such asmicrocontroller 420.

As described above, a host of physiological conditions may benefit froma responsive vascular therapy. Accordingly, at block 702, at least onephysiological condition is detected. The physiological condition(s) maybe circumstances that trigger a cardiovascular controller 438 to takeresponsive action. For example, detecting a bodily movement into a moreupright position coupled with a sudden drop in blood pressure sustainedover an interval may trigger a vascular therapy for orthostatichypotension.

A physiologic interpreter 502 may be employed to detect physiologicalconditions or changes relevant to therapy. For example, a period oflower limb inactivity that exceeds a set threshold may trigger anongoing detection of a segment of the recurring cardiac cycle. Each timethe repeating segment of the cardiac cycle is detected, the vasculartherapy controller 506 stimulates vasoconstriction to augment pumping ofblood in the limbs.

At block 704, a magnitude of a vascular response to the detectedphysiological condition or change is determined. A vascular response ofvasoconstriction may be achieved by electrically stimulating asympathetic nerve, but achieving a vascular response of vasodilation byelectrically stimulating a parasympathetic nerve could also be employedin some implementations. A vascular correlation table 510 may relate amagnitude of the physiological condition or change to a magnitude of avascular response. In other implementations, the relation between aphysiological condition and a vascular response may be determinedalgorithmically or calculated in real time by an engine.

Since the stimulation is typically by electrical pulses, e.g., via leadsof the device 100, the values of the electrical parameters aredetermined as part of determining the vascular response. A vascularstimulation selector 512 may determine voltage, energy, and duration ofpulses to be applied as well as frequency of pulses and duration of atrain of pulses. The vascular stimulation selector 512 may alsodetermine whether to apply the pulses as a pulse train or in bursts.

At block 706, stimulation for achieving the vascular response is appliedto a nerve. An exemplary nerve for achieving vasoconstriction on asystemic level is the greater splanchnic nerve 200 which innervates theabdominal splanchnic vascular bed and the adrenal glands. This vascularbed is thought to be one of the major effectors used by the baroreceptorreflex for achieving an increase in blood pressure. Not only doesstimulation of this nerve cause massive vasoconstriction of abdominalblood vessels, but it also appears to actuate a release epinephrine fromthe adrenals, that further produces global vasoconstriction as well asbronchodilation and other effects of sympathetic stimulation.

At block 708, a physiological effect or result of providing a vascularresponse is detected. A physiologic interpreter 502 includes or hasaccess to physiologic sensors 470 for the detection. The physiologicalresult to be detected should have some relevance to the physiologicalcondition being treated by the device 100.

At block 710, the vascular response is dynamically adjusted based on theeffect detected at block 708. In other words, the vascular therapycontroller 506 and the physiologic interpreter 502 are components of afeedback circuit that is similar to the body's own feedback mechanismsfor maintaining homeostasis. An adjusted therapy, of course, is usuallyproportional to the detected change in a physiological condition. Thus,the provided vascular therapy backs off as the condition improves.

FIG. 8 shows an exemplary process 800 for dynamically providing avascular response to orthostatic hypotension. This process 800 may beimplemented in connection with a suitable device, although herein it isdescribed as being executed by the exemplary implantable device 100 ofFIGS. 1-6. In the flow diagram of FIG. 8, the operations are summarizedin individual blocks. The operations may be performed in hardware and/oras machine-readable instructions (software or firmware) that can beexecuted by a processor, such as microcontroller 420.

At block 802, the device 100 may perform ongoing monitoring of bodilyposition and blood pressure, or may have the capacity to activate ablood pressure sensor if body position meets certain criteria. At block804, in order to check for triggering circumstances, the method 800checks for a recent posture change to a more upright position. If such aqualifying change in body position has occurred, then at block 806 themethod 800 checks for a concomitant sudden decrease in blood pressure ofat least 10 mmHg. If the blood pressure drop is sustained over a timeinterval during which a healthy baroreceptor response would haveintervened to restore satisfactory blood pressure, then at block 808 themethod 800 determines a vascular therapy response that is proportionalto the magnitude of the triggering change in blood pressure. At block810, the vascular therapy determined at block 808 is applied, e.g., as atrain of electrical pulses, to the greater splanchnic nerve 200 toeffect a vasoconstrictive response. The duration of the therapy applieddetermines when a subsequent evaluation of the effectiveness of thetherapy will be performed.

At block 812, the method 800 may additionally determine a cardiactherapy based on the vascular therapy determined at block 808. When themethod 800 is executed by device 100, then in some implementations acardiac therapy controller 518 is subservient to a vascular therapycontroller 506. That is, the values of the electrical and timingparameters for a cardiac stimulation response are derived from thevalues of the electrical and timing parameters determined for a vascularstimulation response. At block 814, the cardiac therapy determined atblock 812 is applied, e.g., as cardiac pacing pulses, to the heart toaugment the vasoconstrictive response being applied at block 810. Thelength of the therapy applied determines when a subsequent evaluation ofthe effectiveness of the therapy will be performed and generally matchesthe duration of the vascular therapy.

Conclusion

Although exemplary methods, devices, systems, etc., have been describedin language specific to structural features and/or methodological acts,it is to be understood that the subject matter defined in the appendedclaims is not necessarily limited to the specific features or actsdescribed. Rather, the specific features and acts are disclosed asexemplary forms of implementing the claimed methods, devices, systems,etc.

What is claimed is:
 1. A method, comprising: detecting a sudden andsustained change in blood pressure; relating the change in bloodpressure to vascular stimulation parameters for executing a vasculartherapy; directly electrically stimulating a sympathetic nerve toachieve the vascular therapy using said vascular stimulation parameters;determining a cardiac response to the change in blood pressure based onsaid vascular stimulation parameters; correlating the cardiac responseto cardiac stimulation parameters that can effectuate the cardiacresponse; electrically stimulating a heart to achieve the cardiacresponse using the cardiac stimulation parameters; detecting an effectof the stimulation of the sympathetic nerve and the heart; and adjustingthe stimulation of the sympathetic nerve and the heart based on theeffect.
 2. The method as recited in claim 1, wherein relating the changein blood pressure to vascular stimulation parameters for executing avascular therapy comprises executing an algorithm relating the change inblood pressure to parameters for executing a vascular therapy.
 3. Themethod as recited in claim 1, wherein relating the change in bloodpressure to vascular stimulation parameters for executing a vasculartherapy comprises using a correlation table that associates a change inblood pressure with stimulation parameters for executing a vasculartherapy.
 4. The method as recited in claim 3, wherein the correlationtable contains precalculated relationships between multiple intermediatevariables.
 5. The method as recited in claim 1 further comprisingdetermining subsequent changes in blood pressure at regular intervalsand relating at regular intervals said changes in blood pressure tovascular stimulation parameters for executing a vascular therapy.
 6. Themethod as recited in claim 1, wherein the vascular stimulationparameters comprise at least one of a voltage, energy, duration ofpulses, frequency of pulses, trail of pulses, burst, and a duration of atrain of pulses.
 7. The method as recited in claim 1, wherein thevascular therapy comprises a degree of vasoconstriction to compensatefor the change in blood pressure.
 8. The method as recited in claim 1,wherein said stimulating a sympathetic nerve comprises providingelectrical pulses to a greater splanchnic nerve to substitute for abaroreceptor reflex response to orthostatic hypotension.
 9. The methodas recited in claim 1, wherein said vascular stimulation parametersinclude electrical parameters for a pulse train to be applied to thegreater splanchnic nerve, wherein the electrical parameters include apulse voltage, a pulse energy, a pulse duration, and a number of pulsesin the pulse train.
 10. The method as recited in claim 1, wherein saiddetecting an effect of the stimulation of the sympathetic nerve and theheart comprises detecting a subsequent change in blood pressure.
 11. Themethod as recited in claim 1, wherein said adjusting the stimulation ofthe sympathetic nerve and the heart based on the effect comprisesadjusting one or more electrical parameters for a pulse train to beapplied to the greater splanchnic nerve.
 12. The method as recited inclaim 1, wherein the cardiac response comprises a cardiac pacing rate toaugment said stimulating the sympathetic nerve.
 13. The method asrecited in claim 1, further comprising detecting a recurring segment ofa cardiac cycle.
 14. The method as recited in claim 13, wherein saidelectrically stimulating the sympathetic nerve is performed with eachoccurrence of the recurring segment of the cardiac cycle.
 15. The methodas recited in claim 13, wherein said electrically stimulating asympathetic nerve is performed with each occurrence of the recurringsegment of the cardiac cycle and timed to reinforce elastic contractionof arterial walls during each transition from systole to diastole. 16.The method as recited in claim 13, wherein determining a cardiacresponse to the change in blood pressure comprises using a cardiaccorrelation table relating the vascular response parameters to cardiacstimulation parameters in order to effectuate a cardiac therapy.
 17. Themethod as recited in claim 1, wherein correlating the cardiac responseto cardiac stimulation parameters comprises using a cardiac correlationtable comprising precalculated relationships between relatedintermediate parameters that link the orthostatic hypotension to valuesfor electrical parameters for applying augmentative cardiac stimulation.18. The method as recited in claim 1, wherein correlating the cardiacresponse to cardiac stimulation parameters comprises using a engine thatruns an exemplary cardiac correlation algorithm, relating the proposedcardiac response to electrical parameters for effectuating the response.19. The method as recited in claim 1, wherein correlating the cardiacresponse to cardiac stimulation parameters comprises using a cardiaccorrelation table relating the vascular response parameters to cardiacstimulation parameters.
 20. The method as recited in claim 1, whereinthe cardiac stimulation parameters comprise and least one of a pacingpulse amplitude, pulse duration, electrode polarity, rate, sensitivity,automatic features, arrhythmia detection criteria, and the amplitude,waveshape and vector of each shocking pulse to be delivered to thepatient's heart.
 21. A method, comprising: detecting a sudden andsustained change in blood pressure; relating the change in bloodpressure to vascular stimulation parameters for executing a vasculartherapy; directly electrically stimulating a sympathetic nerve toachieve the vascular therapy using said vascular stimulation parameters;determining a cardiac response to the change in blood pressure based onthe change in blood pressure and said vascular stimulation parameters;correlating the cardiac response to cardiac stimulation parameters thatcan effectuate the cardiac response; electrically stimulating a heart toachieve the cardiac response using the cardiac stimulation parameters;detecting an effect of the stimulation of the sympathetic nerve and theheart; and adjusting the stimulation of the sympathetic nerve and theheart based on the effect.
 22. The method as recited in claim 21,wherein relating the change in blood pressure to vascular stimulationparameters for executing a vascular therapy comprises executing analgorithm relating the change in blood pressure to parameters forexecuting a vascular therapy.
 23. The method as recited in claim 21,wherein relating the change in blood pressure to vascular stimulationparameters for executing a vascular therapy comprises using acorrelation table that associates a change in blood pressure withstimulation parameters for executing a vascular therapy.
 24. The methodas recited in claim 23, wherein the correlation table containsprecalculated relationships between multiple intermediate variables. 25.The method as recited in claim 21 further comprising determining changesin blood pressure at regular intervals and relating at regular intervalssaid changes in blood pressure to vascular stimulation parameters forexecuting a vascular therapy.
 26. The method as recited in claim 21,wherein the vascular stimulation parameters comprise at least one of avoltage, energy, duration of pulses, frequency of pulses, trail ofpulses, burst, and a duration of a train of pulses.
 27. The method asrecited in claim 21, wherein the vascular therapy comprises a degree ofvasoconstriction to compensate for the orthostatic hypotension.
 28. Themethod as recited in claim 21, wherein said stimulating a sympatheticnerve comprises providing electrical pulses to a greater splanchnicnerve to substitute for a baroreceptor reflex response to orthostatichypotension.
 29. The method as recited in claim 21, wherein saidparameters include electrical parameters for a pulse train to be appliedto the greater splanchnic nerve, wherein the electrical parametersinclude a pulse voltage, a pulse energy, a pulse duration, and a numberof pulses in the pulse train.
 30. The method as recited in claim 21,wherein said detecting an effect of the stimulation of the sympatheticnerve and the heart comprises detecting a subsequent change in bloodpressure.
 31. The method as recited in claim 21, wherein said adjustingthe stimulation of the sympathetic nerve and the heart based on theeffect comprises adjusting one or more electrical parameters for a pulsetrain to be applied to the greater splanchnic nerve.
 32. The method asrecited in claim 21, wherein the cardiac response comprises a cardiacpacing rate to augment said stimulating the sympathetic nerve.
 33. Themethod as recited in claim 21, further comprising detecting a recurringsegment of a cardiac cycle.
 34. The method as recited in claim 33,wherein said electrically stimulating the sympathetic nerve is performedwith each occurrence of the recurring segment of the cardiac cycle. 35.The method as recited in claim 33, wherein said electrically stimulatinga sympathetic nerve is performed with each occurrence of the recurringsegment of the cardiac cycle and timed to reinforce elastic contractionof arterial walls during each transition from systole to diastole. 36.The method as recited in claim 21, wherein correlating the cardiacresponse to cardiac stimulation parameters that can effectuate thecardiac response comprises using a cardiac correlation table comprisingprecalculated relationships between related intermediate parameters thatlink the orthostatic hypotension to values for electrical parameters forapplying augmentative cardiac stimulation.
 37. The method as recited inclaim 21, wherein correlating the cardiac response to cardiacstimulation parameters that can effectuate the cardiac responsecomprises using a engine that runs an exemplary cardiac correlationalgorithm, relating the proposed cardiac response to electricalparameters for effectuating the response.